RAS Inhibitors SG Flashcards
When are ACE inhibitors very effective? What conditions might limit the responsiveness to ACE inhibitors?
Large response
- Pts with ↑ed RAS activation
Decreased response
- RAS suppression due to volume expansion: mineracortocid use, primary aldosteronism, eating a ton of licorice
Why do you tell HF pts NOT to take NSAIDs?
↑risk HF relapse!!!
Blocks PG synthesis - impt for renal compensation during HF
Drug interaction between ibuprofen and diuretics
Ibuprofen ↑Na load
Can ↓effectiveness of diuretic
Can HF pts take aspirin for antiplatelet use or no cause you said no NSAIDs?
Yes to baby aspirin - low dose is still beneficial as anti-platelet med
NO to aspirin doses for everyday pain
- Impair PG synthesis
Even though BBs are often use post-infarction, what is the risk/what pts might you not do this for?
Exacerbate chronic asthma
Why no RAS inhibitors for renal artery stenosis pts
Can cause renal faiure
↓AGT2 mediated efferent arteriole constriction + ↓renal BF = inadequate GFR
SE of ACE inhibitors
Dry cough
Angioedema - can happen anytime during therapy, when start or years after successful treatment
If HF pt complains of wet cough, should you take them off ACE inhibitors?
NO
Productive cough = volume overload
Not ACE inhibitor rxn
How do aldosterone levels change with ACE inhibitors?
+ ACE inhibitor
Initial ↓aldosterone
Escape for longterm HF –> ↑aldosterone which ↑risk CV remodeling
Long term management:
ACE inhibitor + mineralcorticoid receptor blocker
SE of spironolactone
Hyperkalemia
Male impotence
Female amenorrhea
↓chances by using eplerenone
Drug for pharm stress test
Dobutamine
What is neprilysin
inactivates natiuretic peptides
Possible drug target as you try to increase ANP
Neprilysin + ACE inhibitor or ARB?
Nep + ARB
Both Nep & ACE inhibitors have SE of angioeema
